Key Product Details

Species Reactivity

Validated:

Human

Applications

Immunocytochemistry/ Immunofluorescence, Immunoprecipitation, Western Blot

Label

Unconjugated

Antibody Source

Monoclonal Mouse IgG2B Clone # 9B10

Format

BSA Free

Concentration

2.0 mg/ml

View all MAD1L1 Antibodies »

Product Summary for MAD1L1/MAD1 Antibody (9B10) - BSA Free

Immunogen

Recombinant full length human MAD1 protein. Uniprot accession no. Q9Y6D9

Reactivity Notes

Cross-reacts with Human. Not yet tested in other species.

Localization

Nuclear

Specificity

MAD1 (9B10)

Clonality

Monoclonal

Host

Mouse

Isotype

IgG2B

Theoretical MW

~85 kDa.
Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors.

Scientific Data Images for MAD1L1/MAD1 Antibody (9B10) - BSA Free

Western Blot: MAD1L1/MAD1 Antibody (9B10)BSA Free [NB120-5783]

Western Blot: MAD1L1/MAD1 Antibody (9B10)BSA Free [NB120-5783]

Western Blot: MAD1L1/MAD1 Antibody (9B10) - BSA Free [NB120-5783] - Whole extract of HeLa cells was separated on SDS-PAGE and probed with Anti-Mad1 antibody, Mouse monoclonal. The antibody was developed using 1:10000 Anti-Mouse IgG (Fab specific)-Peroxidase antibody produced in Goat.Lanes:1. 1:1000 antibody2. 1:2000 antibody3. 1:4000 antibody4. Negative control

Applications for MAD1L1/MAD1 Antibody (9B10) - BSA Free

Application
Recommended Usage

Immunocytochemistry/ Immunofluorescence

10-20 ug/ml

Immunoprecipitation

1:10-1:500
Please Note: Optimal dilutions of this antibody should be experimentally determined.

Formulation, Preparation, and Storage

Purification

Protein A or G purified

Formulation

10mM PBS (pH 7.4)

Format

BSA Free

Preservative

0.9% Sodium Azide

Concentration

2.0 mg/ml

Shipping

The product is shipped with polar packs. Upon receipt, store it immediately at the temperature recommended below.

Stability & Storage

Store at 4C short term. Aliquot and store at -20C long term. Avoid freeze-thaw cycles.

Background: MAD1L1

Mitotic checkpoint prevents the transition of eukaryotic cells to anaphase until all the chromosomes have made productive, bipolar attachments through their kinetochores to the microtubules of the mitotic spindle. In Saccharomyces cervisiae six genes are important for the kinetochore-dependent mitotic checkpoint: MAD1, MAD2, MAD3, BUB1, BUB3, and Spindles gene MPS1. All six genes have homologues in higher eukaryotes.1-3 In mammals the mitotic checkpoint is an important mechanism that controls the advance to anaphase during every mitosis. Gene inactivation of MAD2 or Bub3 causes lethality in mice and acquisition of aneuploidy in cell culture. Unattached kinetochores are responsible for generating the checkpoint signal that prevents progression to the anaphase stage. Part of the signal is to inhibit the Cdc20-activated form of a ubiquitin ligase, inhibition of the anaphase promoting complex/cyclosome (APC/C) and inhibition of the ubiquitination of substrates whose destruction is important for the cell to advance to the anaphase stage. Human Mad1 can complex with Mad2 and is preferentially localized to unattached kinetochores during mitosis. Both Mad1 and Mad2 localize to the nuclear pore complex throughout interphase.1-3

Long Name

MAD1 Mitotic Arrest Deficient-Like 1

Alternate Names

HsMAD1, MAD1, PIG9, TP53I9, TXBP181

Entrez Gene IDs

8379 (Human)

Gene Symbol

MAD1L1

Additional MAD1L1 Products

Product Documents for MAD1L1/MAD1 Antibody (9B10) - BSA Free

Product Datasheets

Certificate of Analysis

To download a Certificate of Analysis, please enter a lot number in the search box below.

Download SDS

Product Specific Notices for MAD1L1/MAD1 Antibody (9B10) - BSA Free

This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.

Privacy and Cookie Policy
Site Map
© Copyright 2024 Bio-Techne. All Rights Reserved.